ArticleMolecular and cellular biology2012
Mechanistic basis for RAG discrimination between recombination sites and the off-target sites of human lymphomas.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- RAG-mediated structural variation and its impact on relapse risk in acute lymphoblastic leukemia.medRxiv : the preprint server for health sciences · 2026Article
- Recombination between fragile regions associated with chromosomal rearrangements in glioblastoma can be mediated by RAGs.iScience · 2025Article
- Building a neural network model to define DNA sequence specificity in V(D)J recombination.Nucleic acids research · 2025Article
- Early-life tobacco exposure is causally implicated in aberrant RAG-mediated recombination in childhood acute lymphoblastic leukemia.Research square · 2024Article
- Artemis inhibition as a therapeutic strategy for acute lymphoblastic leukemia.Frontiers in cell and developmental biology · 2023Article
- Two Mutually Exclusive Local Chromatin States Drive Efficient V(D)J Recombination.Cell reports · 2016Article
- An interdomain boundary in RAG1 facilitates cooperative binding to RAG2 in formation of the V(D)J recombinase complex.Protein science : a publication of the Protein Society · 2015Article
- An autoregulatory mechanism imposes allosteric control on the V(D)J recombinase by histone H3 methylation.Cell reports · 2015Article
- Histone methylation and V(D)J recombination.International journal of hematology · 2014Review
- Modeling of the RAG reaction mechanism.Cell reports · 2014Article
- Real-time monitoring of RAG-catalyzed DNA cleavage unveils dynamic changes in coding end association with the coding end complex.Nucleic acids research · 2012Article
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4 authors.
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Abstract
During V(D)J recombination, RAG targeting to correct sites versus off-target sites relies on both DNA sequence features and on chromatin marks. Kinetic analysis using the first highly active full-length purified RAG1/RAG2 complexes has now allowed us to define the important catalytic features of this complex. We found that the overall rate of nicking, but not hairpinning, is critical for the discrimination between correct (optimal) versus off-target (suboptimal) sites used in human T-cell lymphomas, and we show that the C-terminal portion of RAG2 is required for this. This type of kinetic analysis permits us to analyze only the catalytically active RAG complex, in contrast to all other methods, which are unavoidably confounded by mixture with inactive RAG complexes. Moreover, we can distinguish the two major features of any enzymatic catalysis: the binding constant (K(D)) and the catalytic turnover rate, k(cat). Beyond a minimal essential threshold of heptamer quality, further suboptimal heptamer deviations primarily reduce the catalytic rate constant k(cat) for nicking. Suboptimal nonamers reduce not only the binding of the RAG complex to the recombination site (K(D)) but also the catalytic rate constant, consistent with a tight interaction between the RAG complex and substrate during catalysis. These features explain many aspects of RAG physiology and pathophysiology.
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